This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Bats are natural host reservoirs for a variety of viruses, many of which are responsible for significant illness and mortality in humans, livestock and companion animals. Although bats may be persistently infected with many viruses, they rarely display clinical symptoms. Thus, bats appear to be able to co-exist with viruses and may have evolved mechanisms to rapidly control viral replication while still allowing transmission and occasional spillover to more susceptible species. In contrast to the ability of bats to tolerate viruses, the recent discovery of white nose syndrome (WNS), a fungal disease that has resulted in the devastation of some Northeastern US bat populations has revealed a potential susceptibility of bats to fungal diseases. Despite the devastation of bats due to WNS, and their central role in harboring and transmitting viral diseases, there is currently little information on the immune system of bats and few reagents exist to study the bat's immune response. Information on the immune response of bats would provide important insights into how bats escape the clinical manifestations of viral infection and the reasons for their susceptibility to WNS. In this proposal we are using the black flying fox, Pteropus alecto as a model to investigate the role of the interferon (IFN) response in antiviral immunity in bats to determine whether differences in the IFN response contribute to the ability of bats escape the clinical manifestations of disease following viral infection.